test 4 level 3
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| 2 major disorders of stomach and UPPER small intestine? | Gastritis and Peptic ulcer disease
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| an inflamtion of the gastric mucosa is one of the most common problems affecting the stomach | Gastritis
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| gastritis may be clasified as ? | acute or chornic and diffuse or locaziled
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| occurs as a result of a breakdown in the normal gastric mucosal barrier. | Gastritis
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| protects the stomach tissue from the corrosive action of HCL acid and pepsin | Function of gastric mucosal barrier
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| In gastritis when the mucosal barrier is broken, HCL acidm and pepsin can diffuse back into the mucusa resulting in? | tissue edema, disruption of cappilary walls with loos of plasma into gastric lumen and possibly hemmorhage
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| Drugs that contribute to the development of acute/chronic gastritis? | NSAIDS, inlduign aspirin and corticosertiods, as they inhibit prostaglandin(which is protective to GI mucosal wall) and anticoagulants and digoxin
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| Injesting alchol, eating large quanitites of spicy, irriating foods and renal failure can cause? | Gastritis
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| an important cause of chronic gastritis? | Helicobacter pylori
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| Bacterial, viral and funfal infections have been associated with? | chronic gastrites
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| Intense emotional responses and CNS lesion may produce inflmation of mucosal lining as a result of hypersecretion of HCL acid | cause of gastritis
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| Anorexia, nausea, vommiting, epigastric tenderness and a feeling of fullness. Hemmorhage is associated with alchol abuse and at time is the ONLY symptom | S/S of acute gastrits
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| Prognosis of acute gastritis? | Self limiting, lasts a a couple hours or days, complete healing
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| When the parietal cells are lost as a result of atrohy the source of intrinsic factor is lost. | Chronic gastritis and results in cobalmin deficiency/ pernicious anemia
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| A CBC in gastritis may show? | anemia from blood lossor lack of intrinsic factor
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| If vommiting accompanies acute gastritis do what? | rest, NPO status and IV fluids, antimetics
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| treatmet of acute gastiris focuses on reducing irritation of the gastric mucosa and providing symptomatic relief through giving? | PPI's( azoles) or H2 receptor blockers (tidine)
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| Treatment of chronic gastrits? | Antibitotics for H. pylori, colabalmin therapy, non irritating diet w/ six small meals a day
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| drug and alchol abuse think? | gastritis
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| in gastritis check stool for? | occult blood
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| a severe case of acute gastritis may require? | NG tube for lavage
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| Neutralize acid in stomach and esophagus, rapid onset and short effect | Antacids
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| When give antacids? | before a meal
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| Reduce gastric HCL secretion, slower onset longer duration | H2 receptor blockers
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| Inhibits gastric acid secretion has a prolonged effect | Proton pump inhibitor
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| smoking is contraindicated in? | all forms of Gastritis
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| A condition charecterized by errosision of the GI mucosa resulting from digestive action of HCL acid a pepsin | Peptic ulcer disease
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| What part of GI tract is suspetible to ulcer development? | Any portion of the GI tract that comes into contact with gastric secretions
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| How are petic ulcers classified? | acute or chronic
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| accoiated with superficial erosion and minimal inlamation, resolves quickly when the cause is removed | The acute ulcer
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| eroding throguh the musclular wall with the formation of fibrous tissue | A chronic ulcer
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| peptic ulcers develop only in an? | acidic enviorment
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| histamine in released from the damaged mucosa, resulting in vasodilation and increased cappilary permeability in peptic ulcers results in? | further secretion of acid and pepsin
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| In adition to chronic gastritic H pylori is associated with? | peptic ulcers
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| alters gastric secretion and produces tissue damage leading to? | peptic ulcer disease
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| Aspirin and NSAIDS inhibit prostaglandis, increase gastric acid secretion and reduce the integrity of the mucosal barrietr | Ulcerogenic drufs
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| Coffe and alchol | Stimulate gatric acid production this Peptic ulcers
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| stress affects what in ulcers? | The healing of them
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| gastric ulcers are most commonly found in the? | Antrum
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| Gastric ulcers are more likely than duodenal ulcers to result in? | Obstruction
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| H.Pylori, meds, smoking and bile reflux are R/F for? | Gastic ulcers
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| Most common ulcer? | Duodenal
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| Most common cause of duodenal ulcer? | H. pylori
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| high epigastrum pain, occurs 1-2 hours after meals, pain is burning, if ulcer has eroded through mucosa food agravates this | Gastric ulcer
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| Occurs when gastric acid comes in contact with the ulcers/ With meal ingestion food is present to help buffer the acid, symptoms occur 2-5 hours after a meal, pain is burning and is midepigastrum and possible back pain antacids /h2 receptor block fix S/S | Duodenal ulcers
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| Tendencey to occur continously for a few weeks or months and then disaper for a time then recurs | Duodenal ulcers
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| Older adults and ulcers | usually siletn
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| Three major complications of PUD? | Hemorrhafe, perforation and gastric outlet obstruction, EMERGENCIES
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| Hemmorahfe is the more common in | Duodenal ulcers
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| Most lethal complication of PUD? | Perferation
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| the ulcer penetraties the serosal surface with spillage of either gastric or fuadenal contents into the periotenal cavity | Perferation
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| Sudden severe upper abdominal pain that quickly spreads throughout the abdomen. The pain radates to the back and is not relievedd byt food or antacids | Perforation
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| Bowel sounds usally absent, absomen appears rigid and boardlike tachy/ HISTORY of ulcer disease or recurrent symptoms of indigestion | [erforation
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| if perforaiton is untreaed bacterial periotnitis may occur within? | 6-12 hours
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| obstruction in the distal stomavh and duodenum is the result of what in regards to PUD? | edema, inflamation or pylorspasm and fibrous scar tissue formation
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| how can relief be obtained with gastric out obstruction due to PUD? | belching or self-induced vommiting
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| Vomit that contains food particles that were injested hours or days before the vommiting episode signals? | Gastic outlet obstrcution due to PUD
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| most accurate diagnostic procedure for PUD? | Endoscopy
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| Eoscopy with biopsy is used in PUD to rule out? | H. Pylori
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| no invasive tests for H. Pylori? | Stool or breath test.
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| A CBC in PUD? | may show anemia
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| A serum amlyasyse determination s done to determine _______________ when posterior duodenal ulcer penetration of the pancreas is suspected | Pacreatic
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| aim of treatment with PUD? | Decrease gastric acidity and enhnace mucosal defense mechanisms
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| Pain from ulcers disaper in? | 3-6 days but not heal till 3-9 weeks
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| important follow up for PUD? | follow up endoscoppy
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| Patietns with H. Pylori are treated with? (and PUD) | Antibiotics and PPI
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| with PUD it is important to stop? | smoking
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| Because ulcers frequently recur, interupption or discontinuation of therapy can have? | harmfull results so encourage continuing and follow up
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| H2 receptor blockers and PPIs may be stopped after? | the ulcer has healed or used as low dose maintance
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| This promotes ulcer healing, onset is one hour and lasts 12 hours | H2 receptor blockers
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| More effective than others in reducing gastric secretion and promoting ulcer healing | Proton pump inhibiros
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| These increase gastric Ph by neutralzaing the HCL acid. magnesium hydroxide or aluminum hydroxide | Antacids
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| Whent take antacids | after meals so they last a long time
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| If Ph is less than 5 with PUD consider? | NG suction
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| used for short term treatment of ulcers. It proovides cytoprotection for the esophagus, stomach and duodenum, should be given 30 minutes before an antacid. | Sucrafate
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| what antidepressants for PUD? | Tricylic
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| DIet for PUD? | No caffeine, no aclhol, do bland diet, (no broth tho)
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| PUD vleeding, increased pain and discomfort and N/V | Acute exacerbation
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| What to do in perferoation? | NG tube for decompression/stop aspiration, volume replacement, antibitoics, pain meds and surgery
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| What to do in gastric outlet obstruction? | Decompress stomach, fix fluid imbalance, clamp tube overnight and see if its still backing up.
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| symtpms related to gastric irritation during PUD? | Epigastric pain
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| Treatment of acute phase of PUD? | NP, NG tube/suction, IV fluid replacement
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| sudden severe abdominal pain, rigid boardlike abdomen, severe generalized abdominal and shoulder pain, fetal position and grunting respirations, bowel sounds ABSENT | perforation
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| direct result of surgical removal of a large portion of the stomach and the pyloric sphincter | Dumping syndrome
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| what is more common acute or chronic PUD? | chronic
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| Pathology of PUD? | Not neccesarly the amount of HCL secreted but the ability of it to penetrate the mucosal barrier
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| pain in high epigastrum | Gastric ulcer
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| pain is burning or gaseous pain is spnontaineous usually 1-2 hours after meals, food can agravate it? | Gastric ulcers
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| occurs 2-4 hours after eating, relieved by antacids or H2 receptor blockers, burning cramplike pain in mid epigastric and may radiate to back | Duodenal ulcers
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| Duodenum ulcers involves the duodenum and the? | pylorus
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| This ulcer pain is often relived by food? | duodenum ulcer
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| serum or whole blood antibody testing including IGg | Does not distinguish between current or past PUD but good still
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| Upper Barium GI contrast studies with gastric analysis may be helpful in diagnosing? | PUD
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| What diet in PUD? according to powerpoint? | 6 bland small meals a day, no spicy, alchol, carbonated beverage/caffeine stop smoking dont take NSAIDS/aspirin
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| Most common complication of PUD? | Hemmorhage
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| sudden sharp severe abdominal/shoulder pain, black or bloody stools bloody vomit that looks like coffee grounds rebound tenderness think? | Perforation
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| In pud, hemmorage, perforation and gastric outlet obstruction are all? | medical emergencies
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| acute ulcers that follow a major physiologic insult | Physiologic stress ulcer
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| dx: for physiologic stress ulcer? | endoscopy
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| prevention of physiologic stress ulcer? | prophylaxis with antisecretory agents
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| treatment of physiologic stress ulcer | reduction of gastric acid secretion with PPI or h2 receptor blockers
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| physiologic stress ulcers occurs most often in? | infants and children
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| Acute inflamtion of the pancreas. varies from mild edema to severe hemorrhagic necrosis | Acute pancreatitis
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| Acute pancreatis is more common in? | Middle aged men and women.
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| race for pancreatis? | more african americans
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| Most common cause of acute pancretitis? | Gallbladder, second is chronic alchol intake
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| Independent risk facto for | acute pancretitis
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| a mixture of cholesterol crystals and calcium salts found in patients with acute pancreatis? | Biliary sludge
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| Formation of bilary sludge is seen in patients with bile? | staiss
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| hypertriglyceridema is associated with | Acute pancretitis
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| most common pathogenic mechanism of acute oancreatis is? | autodigestion of the pancreas
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| Activated trypsin in the __________ can digest the ________ and produce bleeding | Pancreas
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| Edematous or interstial pacreatitis | Mild pancreaitis
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| Necrotizing pancreatitis | Severe pacreatitis
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| Predominant manifestation of acute pancreatitis | Abdominal pain
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| The pain is due to distention , peritoneal irritation and obstruction of the billary tract | Pain in pancreaitis
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| Where is the pain in pancreaittis? | Left upper quadrant, may be midepigastrium radiates to back commonly
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| The pain has a steady onset and is described as severe, deep, piercing and continous or steady, pain is agravated by eating and occurs when recumbnent | Pancreaitis
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| Patient may assume various positions involving flexion of the spine in an attempt to relieve severe pain, may see N/V fever, leukocytosis, hypotension, jaundice, muscle guarding | Pacereatis
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| Bowel sounds in pacreatis? | decreased or absent
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| Paralytic illeuls and crackles of lungs may be present in? | pancreatitis
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| cyanosis or greenish to yellow-brown discolaration of the abdominal wall. | Pancreatisis
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| in pancreatis echmyoses of the flanks | Grey turners, and the periumbical area is cullens
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| Result from seepage of blood stained exufate from the pacreas | Grey turner/cullens, discolorations of abdominal walls
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| Two significant local complications of acute pancreaitis? | Pseudocyst and abscess
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| An acummulation of fluid, pancreatic enzymes, tissue debrs, and inflamatory exudate surronded bt a wall | A pancreatic pseudocyt
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| Palpable epigastric pain is evident of? | pacreatic pseudocyts
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| Serum amlysase levls in pancreatits is? | high
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| Pacreatic pseudocysts can perferoate cuasing | perotonitis
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| A pancreatic absess is a? | collection of pus
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| upper abdominal pain, abdominal mass, high fever and leuko cytosis | pacreatic absess need to treat to prevent sepsis
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| Main systemic complications of acute pancreatis? | pulmonary (pneumonia, ARDS, pleural effusion) and cardiovasculare (hyptension) and tetant thanks to hypocalcemia
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| enzyme induced inflamtion of the diapragm occurs with the end result being? | atelectasis
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| Trypsin in pancreatis puts the patient at risk for? | DIC, thrombi
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| primary diangostic tests for acute pancreatits? | serum amylase and serum lipase
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| Why is serum lipase more important than serum amylase in DX pancreatitis | amylase is raised in other disoreders
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| increase i liver enzymes, increase in trigluycerides and decrease in calcium points to? | pancreatits
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| Goals of tx for acute pancreatits? | Prevent shock, reduce pancreatic secretions, corect FE imbalances, prevent/treat infections, remove cause
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| in aute pancreatis pain meds are given in addition to? | antispasmodics
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| To pevent shock in pacreatis | blood volume replacements are used, like lR
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| It is important to reduce or supress pancreatic enzymes to decrease stimulation of the pancreas and allow it to rest in acute pancreatits how is this accomplished? | NPO, NG suction to reduce vommiting/gastric distention and to prevenet gastric acidic contents from entering the duodenum, PPI'S/antacids
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| In patients with acute necrotizing pancreatitis, what is the leading cause of death? | Infection
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| drugs that cure pancreaitis? | none
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| When food is allowed, in aucte pancreatits what is the diet? | Frequent feedings, high in carbs that is least stimulatinf no alchol
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| is frequent vommiting seen in acute pancreatis? | yes
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| major focus of care in acute pancreatits is? | pain
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| Diet teaching for acute pancreatits includes? | reduction of fat as the stimulare onacreas, carbs are less stimulating
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| If a person with acute pancreatitis recognizes symptoms of infection diabetes or steatorrhea do what? | Call dr.
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| A continous, prolonged inflamatroy and fibrosing of the pancreas, the pancreas is progressivly destroyed as it is replaced by fibroitic tissue | Chronic pancreaitis
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| Strictures and calcifications may occur in the pancreas in what disease? | Chronic pnacreatis
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| Can be due to alchol, obstruction by gall stones, timor, pseudocyts or traumas, disease, autoimmune pancreatis and cystic fiboris, may have NO history of acute condiition | Chronic pancreatis
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| Most common cause of obstructive pancreaitis is? | inflamation of the sphincter of oddi ascociated with gall stones
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| in non obstructive pancreaitis there is inflamtion and sclerosis mainly in the head of the oancres and around the pancreatic duct this type of chronic pancreatiis is the? | most commobn
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| Chronic pancreatits can be caused by those who abuse? | alchol
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| abdominal pain that is heavy gnawing feeling or burning and cramplike, not relived with food, come and goes | Chronic pancreatis
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| Malabsotption with weight loss, consitpation, mild jaundice with dark urine, steatorrhea and diabetes melitys are signs of | Chronic pancreaitis
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| Frothey urine and stool, steatorhea can become severe with vommitius | Chronic pancreatis
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| The level of serum amylase and lipase may be elvated slightly, bilirubin is increased, incresred ESR and mild leukocytosis, alkaline phosphate | Chronic pancreatis
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| Used to visualize the pancreatic and common bile duct | ERCP
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| Deficiency of fat-soluble vitamins, cobalmin, glucose intelerance and dibetes may be found in | chronic pancreaitis
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| Ways to control pancreatic insufficency in chronic pancreatits? | Diet, pancreatic enzyme replacement and control of diabetes, small bland frequent meals, no alchol or caffeine prescribe bile salts to help with fat absorption
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| Pacreatic enzymes are taken with ? | a meal or snack
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| shock/vasodilation is seen in? | acute pancreatis
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| Cavity continous with or surronding outside of pancreas filled with necrotic produts and liquid secretions | pancreatic pseudocytst
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| Large fluid containing cavity within the pnacreas resulting from extensive necrosis in the pancreas | Pancreatic absess
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| urinart amylase may be seen in? | acute pancreatits
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| TPN in acute pancreatis may be needed if there is a ? | severe nutritional defict
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| if enteral feedings are needed in acute pancreatits it is via a ? | jejunal feeeding tube
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| Two major types of chronic pancreatis? | Chronic obstructive pancreaitis, and chronic calcifying pancreatisi
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| chronic pancreatis may be associated with acute? | billary diseae
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| Mild jaundice with dark urine is seen in? | Chronic pancreatits
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| Most common disorder of the bilairy sytem is? | Cholelithias (stones of gallbladdder
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| Where may the gallstones lodge ? | neck of the gallbladder or in the cystic duct.
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| Inflamation of the gall bladder, this is usually associated with choleithiasis (gall stones) | Cholecystis (usually occur with gall stones)
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| Many people with stones are | asymptomatic
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| Cholecystectomy is? | removal of the gall bladder
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| Who is at higher risk for cholilithiasis? | Women, multipara and over 40, oral contraceptives, sedetary lifestyle and obesity. asins
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| Cause of gallstones? | Unknown
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| Develops when the balance that keeps cholesterol, bile salts calcium in solution is altered so that these substances precipitate | Cholelithiasis
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| Conditions that upset the balance of cholesterol, bile salts and calcium in solution | Infection and disturbances in metabolism of cholesterol
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| when bile is supersaturated with cholesterol what occurs? | Gall stones
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| besides cholesterol what 4 things can cause gall stones? | Protein, calcium, bilirumbin and bile salts.
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| Most common gallstone? | mixed predominatly cholsterol
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| stasis of bile as well as changes in composition of bile (bilary sludge) can lead to? | gall stones
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| The gallstones may remain in the gallbladder or migrate to the? | cystic duct or the common bile duct
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| Gallstones cause pain as they? | pass through the ducts and produce an obstruction
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| What size gallstones are more liekly to produce an obstruction | Smalls
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| if blockage of gallstone is in cytic duct? | bile can still get though
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| Choleosytisi is most commonly associated with? | obstruction caused by gallstones or billary sludge
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| asccoiated with prolonged immobility, elderly, diabetes and prolonged PN? | Just choleocytis
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| The gallblader is edmeatous and hypermic and may be distended with bile or pus | During an acute attack of cholecystits
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| When a stone is lodged in the ducts or when stones are moving through the ducts, | spasms may result
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| bilarly colic, pain is often steady, pain can be excurtating and accomponied by tachy , diaphoresis, may last up to an hour | Cholelithiasis
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| When the pain of cholethiasis subsides resuldual tenderness is felt in the? | right upper quadrant
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| The attacks of pain from gallstones occurs 3-6 hours after? | a high fatty meal or patient lays down
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| dark amber urine, obsructive jaundice, clar colored stools, bleeding tendencies, steatorheaa | Total obstrutction by gall stones related to bilary obstruction
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| indgestionand pain / tendeness in right upper quadrant | Choliethesiais
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| History of fat intoleracne, dyspesia, heartburn and flatulence | Chronic Chlecytutus
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| Most common complications of choleysitis in older or diabetic | Gangrenous cholecytisi and bile peritonits
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| Commonly used to dx gallstones? grear id allergic to contrast! | ultrasound
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| Allows visualaztion of the gall bladder , the cystic duct, the common hepatic duct and the common bile duct, bile taken during this is sent for culture. | ERCP
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| Insertion of a needle directly into the gallbladder duct followed by injection of contrast | Percutaneous transhepatic cholangiography
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| WBC in choleothasis? | increased
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| Blood levels elevated in cholestais? | ALT, AST, and alkaline phosphate
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| Once gallstones become syptmotic do what? | Surgical intervention with cholecystectomy
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| during an acute episode of cholecystits, treatment focus on? | pain control, control of possible infection with antibiotics and maintece of FE NG insertion of N/V is severe
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| may be used to drain purluent material from the obstructed gallbladder | a cholecysstostomy
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| Treatment of choice for symptomatic cholethiasis | Laproscoprtic cholecystectomy
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| able to return to work how long after choleystecomy? | a week
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| Common complication in laproscopic cholestectomy? | Injury to common bile duct
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| most common drrugs used in the treatment of gallbladder disease? | Analgesics, anticholinergics(antispasmodics) , fat soluble vitamins and bile salts
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| fat soluble vitamis needed if? | bilary tract is obstructed
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| Nutrition during acute gallbladder disease? | Small frequent meals with some fat at end of meal to increase gallblader emptying
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| After laproscopic cholestrectomy nuttrition adive? | Eat nutrion foods avoid fat for 4-6 weeks
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| jaundice, clay colored sools, dark foamy urine, steatorhea, fever and increased WBC count | Bilary tract obstruction
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| bleeding may result in cholesthiasis from | decreased prothrombin time thus take care during injections
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| abdominal pain and fever may indicate? | Pancreaitis
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| A common complication postop from laparscopic chlecystectomy is? | shoulder pain
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| how help with shoulder pain after a lap choleystectomy? | SIMS position, nsaids/codeine
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| after surgery for gallstones as well as acute period? | avoid exess fat
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| inflamation to mucosa lining or entire wall of gallblader, edmea | CholthiatITIS
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| absess, pancreatis, cholingitis, billary cirhosis and fistula are common complications of? | Gallbladder disease
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| in gallbladder disease what is a major complication if not treated? | rupture of gallblader resulting in peritonitis
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| antimetics are often given in? | choliethithais
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| ESWL | can use a lithiotripter to break apart a gallstone
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